neurotransmitter gaba
Uploader Comments (altruist78)
All Comments (46)
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@KimberlyBSPhD Re: Gaba as an inhibitor. Forgive my layman's understanding, however as to your response stating that it is important to understand the properties of agonists and antagonists. If GABA binds to the receptor site and reduces the propensity for an action potential at the post synaptic neuron, is this not then antagonistic given the failure to activate the physiological response, i.e. the action potential. Why in the animation is the action potential continuing? Thanks in advance
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I appreciate the conversation that took place between @almostskater3210 and @laaxe regarding the benzodiazepine withdrawal syndrome as, even after having done a careful taper off of Klonopin, I am still suffering greatly at almost 16 months after my final dose. Like many of us in similar circumstances, I seek to understand why.
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@almostskater3210 They do not want to talk to me about it. They know that I can use telepathy, Randi know that.
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@almostskater3210 Thanks, my friend. What you've already posted has me looking at the benzo in a different light already. Now I've got to word it in a fashion the scientifically challenged will understand; a challenge in itself!
Greatly appreciated!
Thanks again!
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I agree with you in every way; so many drugs are overprecribed. Various SSRIs are prescribed for depression of any kind when they were showed to be clinically insignificant except in severe depression.And they don't stress the risks of long term benzo use. But your welcome; and if you have any questions on neuropsychopharmacology, feel free to ask anytime, and I'll see if I can help. If I find any conclusive info. on the neurochemistry of benzodiazepine dependence, I will let you know.
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@almostskater3210 I (and many others) would be profoundly grateful for any knowledge you could help with. This is a huge sticking point, as most GP's & psychiatrists haven't a clue as to why benzodiazepine withdrawal syndrome, or protracted withdrawal syndrome occurs after a rapid taper from benzos, which more often than not, lasts for years. Unfortunately, over 100 million prescriptions are written yearly in the US (a DEA stat), which is approaching insanity in my opinion. But sincere thanks!
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so you may be partially correct in that gene expression could be changed, causing seriously low GABA production, although I doubt that is the case as synthesis of neurotransmitters is relatively "simple" and very controlled. All of this is speculation and I will need look at some literature. Antibodies with an attached fluorophore can be used to seek out specific enzymes. If a brain of an benzodiazepine dependent person was stained with a certain antibody, one could look at GAD levels.
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...(continued) but the reason benzo withdrawal lasts for such a long time might be from other changes in neurochemistry/anatomy. Epigenetics displays great promise in explaining this phenomenon, as changes in gene-expression are often the long-term regulators of many neurochemicals. I would guess that maybe changing GAD gene expression (GAD is the enzyme that synthesizes GABA from glutamate) or expression of some other GABAergic constituent might cause long-term dysregulation .
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Benzodiazepine dependence is caused neurons decreasing their concentration of GABA receptors (decreased inhibition), preventing chloride ion flow; however, NMDA receptors are upregulated to a lesser extent (increased excitation) lending to the drug's withdrawal syndrome. This glutamate rebound can also cause excitotoxicity in theory, and excitotoxicity does happen during alcohol withdrawal because alcohol primarily antagonizes NMDA while agonizing GABA to a lesser extent.
and vasopressin
altruist78 3 years ago
ok thnx for the info ...
altruist78 3 years ago